Allan Struthers

Biography

Allan Struthers graduated MB (Hons) from Glasgow University UK in 1977. After junior hospital posts, he was Senior Registrar at the Royal Postgraduate Medical School and Hammersmith Hospital in London in 1982 – 1985.

He was then appointed Wellcome Senior Lecturer/Consultant Physician in Dundee and is currently Professor of Cardiovascular Medicine and runs the Heart Failure service at Ninewells Hospital in Dundee. He is also an Honorary Professor at St Andrews University Medical School. He was Chairman of the SIGN Guidelines in Heart Failure twice (2007 and 2016) and Chairman of NHS-QIS Standards (2010) for Heart Failure. In addition, he is also Chairman of Tenovus NSAC, Senior Regional Advisor for SACDA and Council member of Chest, Heart and Stroke Scotland.

He is currently Co-Head of the Division of Molecular and Clinical Medicine at the Medical School in the University of Dundee. Professor Struthers runs a large clinical research programme and has supervised 50 MD/PhDs.

He helped pioneer the use of plasma BNP to identify heart failure patients and the use of aldosterone blockers to reduce their mortality. More recently, he is exploring the use of plasma BNP (and troponin) in primary prevention patients to identify silent but treatable heart disease.

Another research interest is in allopurinol and he has recently shown it to delay chest pain on exercise in angina patients and to regress LV Hypertrophy. Ongoing studies are exploring allopurinol in dialysis patients, in COPD patients and in sarcopenic patients.

In total he has held 38 different British Heart Foundation (BHF) grants along with grants from CSO, MRC, Wellcome, HTA and CHSS. He has published 508 papers which are cited around 600 times every year. His research “h” factor is high at 60. He is a Fellow of the European Society of Cardiology (FESC), the Royal Society of Edinburgh (FRSE) and the Academy of Medical Sciences (FMed Sci).

Research

Professor Struthers has repeatedly spotted new therapeutic opportunities and conducted the initial “proof of concept” studies which, led to confirmation in larger trials. For example, he was the first to ever show that aldosterone blockade had beneficial cardiac effects in man on top of ACE inhibitors (Am J Card 1995, 76: 1259): those effects were to reduce both ventricular arrhythmias and cardiac sympathetic activity. This discovery helped lead to the RALES trial where spironolactone reduced mortality in heart failure (HF) by 30%. He also discovered other mechanisms contributing to aldosterone’s ability to increase cardiac deaths, i.e. it decreases endothelial nitric oxide, it decreases cardiac autonomic function and it increases plasma collagen markers (which are a good surrogate for myocardial fibrosis).

A second area where he made important original discoveries is B-type natriuretic peptide (BNP). He wrote one of the two original studies published together in the Lancet (1993) which led to the use of plasma BNP levels to identify heart failure (HF). A later paper by him, also in the Lancet, confirmed this. BNP is now an integral part of all HF guidelines. Professor Struthers has now moved on to make original observations about BNP in a completely new (non HF) area. He has recently discovered that if an apparently healthy individual has a high BNP level, this often signifies that they have silent coronary artery disease (Heart 2006, 92: 487 and 916). This is a major finding as BNP screening could now be used to help identify those many apparently healthy middle aged individuals whose first ever manifestation of their previously silent coronary disease is sudden cardiac death. He has now developed the new concept that primary prevention could be improved by 3P Screening whereby BNP is used to select individuals for detailed cardiac phenotyping followed by personalised medicine against any abnormalities seen on cardiac phenotyping. (JACC 2012, 60, 960-8; Hypertension 2013, 62, 236-9).

A whole other area pioneers by him is allopurinol. He developed the novel idea that allopurinol could be "oxygen in a pill" because it inhibits an oxidase enzyme which normally "wastes" oxygen in ischaemic tissue. A recent Lancet paper (2010, 375: 2161 – 7) showing this could lead eventually to the use of allopurinol as an oxygen sparing agent in all ischaemic diseases. He had already unravelled the exact mechanism whereby allopurinol improves endothelial function by profoundly reducing vascular oxidative stress and not at all by decreasing uric acid. This was a much debated issue before his elegant paper in Circulation settled the issue. His recent work has also shown that allopurinol regresses LV mass in patients with LV hypertrophy. The above work has now led to an HTA grant to examine the effect of allopurinol on CV events/mortality in ischaemic heart disease (the ALL-HEART study).

Lastly, he had the original idea behind another paper of major therapeutic importance. In conjunction with Professor McMurdo, he showed that ACE inhibitors improve mobility in elderly, disabled, immobile patients, which should greatly improve the quality of life of many elderly patients. In fact, this paper won the Bruce P. Squires award as one of the best in the year. If confirmed, ACE inhibitors could become the equivalent of "exercise in a pill" to the many elderly with limited mobility.

Can we affect CV disease by managing uric acid?, International Symposium: Uric Acid, Gout and Beyond: Is CV Risk a New Objective. Bologna, Italy, 2012

Teaching

He teaches Cardiovascular Medicine and Therapeutics at both the University of Dundee and the University of St Andrews Medical School. He is on Steering Group of the eHEART project of Chest, Heart & Stroke Scotland.

Struthers AD, Lang CC. The potential to improve primary prevention in the future by using BNP/N-BNP as an indicator of silent “pancardiac” target organ damage: BNP/N-BNP could become for the heart what microalbuminuria is for the kidneys. EUROPEAN HEART JOURNAL 2007, 28: 1678-1682. (Impact Factor 10)

Farquharson CAJ, Struthers AD. Gradual reactivation over time of vascular tissue angiotensin I to angiotensin II conversion during chronic lisinopril therapy in chronic heart failure. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2002; 39: 767-775.